Case Report: Atypical hemolytic uremic syndrome triggered by Rhinovirus/Enterovirus infection with cutaneous thrombotic microangiopathy requiring surgical management
4 affiliations
- 1Department of Nephrology, Shanghai Children’s Medical Center, School of Medicine, Shanghai Jiao Tong University , ,
- 2Department of Burns and Plastic Surgery, Shanghai Children’s Medical Center, School of Medicine, Shanghai Jiao Tong University , ,
- 3Department of Pathology, Shanghai Children’s Medical Center, School of Medicine, Shanghai Jiao Tong University , ,
- 4Department of Critical Care Medicine, Shanghai Children’s Medical Center, School of Medicine, Shanghai Jiao Tong University , ,
Abstract
Atypical hemolytic uremic syndrome (aHUS) represents a complement-mediated thrombotic microangiopathy (TMA) characterized by microangiopathic hemolytic anemia, thrombocytopenia, and end-organ damage, most frequently affecting the kidneys. Although infection is a well-recognized precipitant, extensive skin involvement is uncommon. Here, we describe a 14-year-old boy who developed aHUS following Rhinovirus/Enterovirus infection. He was found to have anemia, thrombocytopenia, acute kidney injury, hematuria, and proteinuria, and peripheral smear examination demonstrated schistocytes. Complement evaluation showed reduced C3 and factor I concentrations, increased soluble C5b-9, and preserved ADAMTS13 activity. Investigations for Shiga toxin-producing Escherichia coli, systemic autoimmune disease, and alternative infectious etiologies were negative. Even with eculizumab, corticosteroids, therapeutic plasma exchange (TPE), and continuous renal replacement therapy (CRRT), his condition progressed to petechiae, ecchymoses, hemorrhagic bullae, and necrotic lesions of the axilla, neck, and back. Since the necrotic areas failed to heal and were accompanied by continued platelet consumption and a heightened risk of infection, surgical debridement and wound closure were undertaken after the platelet count reached 81 × 10^9/L. Histopathologic analysis of the excised tissue confirmed cutaneous thrombotic microangiopathy with microvascular thrombosis. Following the procedure, platelet count, hemoglobin, and complement C3 returned to normal, and the wound healed without complication. At subsequent follow-up, the scars were supple and level, with no sensory deficit or functional limitation. This report expands the range of infectious triggers associated with aHUS and demonstrates that persistent necrotic cutaneous thrombotic microangiopathy may necessitate prompt surgical management in addition to complement inhibition and supportive treatment.
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BibTeX
@article{shen2026case,
title = {{Case Report: Atypical hemolytic uremic syndrome triggered by Rhinovirus/Enterovirus infection with cutaneous thrombotic microangiopathy requiring surgical management}},
author = {Jiayao Shen and Kaixuan Cai and Weijie Kang and Qiao He and Jian Zhang and Lei Yin},
journal = {Frontiers in pediatrics},
year = {2026},
month = oct,
doi = {10.3389/fped.2026.1973640},
url = {https://europepmc.org/article/PMC/PMC13724424},
note = {CC BY},
}
RIS
TY - JOUR
TI - Case Report: Atypical hemolytic uremic syndrome triggered by Rhinovirus/Enterovirus infection with cutaneous thrombotic microangiopathy requiring surgical management
AU - Jiayao Shen
AU - Kaixuan Cai
AU - Weijie Kang
AU - Qiao He
AU - Jian Zhang
AU - Lei Yin
PY - 2026
DA - 2026/10/19
JO - Frontiers in pediatrics
DO - 10.3389/fped.2026.1973640
UR - https://europepmc.org/article/PMC/PMC13724424
AB - Atypical hemolytic uremic syndrome (aHUS) represents a complement-mediated thrombotic microangiopathy (TMA) characterized by microangiopathic hemolytic anemia, thrombocytopenia, and end-organ damage, most frequently affecting the kidneys. Although infection is a well-recognized precipitant, extensive skin involvement is uncommon. Here, we describe a 14-year-old boy who developed aHUS following Rhinovirus/Enterovirus infection. He was found to have anemia, thrombocytopenia, acute kidney injury, hematuria, and proteinuria, and peripheral smear examination demonstrated schistocytes. Complement evaluation showed reduced C3 and factor I concentrations, increased soluble C5b-9, and preserved ADAMTS13 activity. Investigations for Shiga toxin-producing Escherichia coli, systemic autoimmune disease, and alternative infectious etiologies were negative. Even with eculizumab, corticosteroids, therapeutic plasma exchange (TPE), and continuous renal replacement therapy (CRRT), his condition progressed to petechiae, ecchymoses, hemorrhagic bullae, and necrotic lesions of the axilla, neck, and back. Since the necrotic areas failed to heal and were accompanied by continued platelet consumption and a heightened risk of infection, surgical debridement and wound closure were undertaken after the platelet count reached 81 × 10^9/L. Histopathologic analysis of the excised tissue confirmed cutaneous thrombotic microangiopathy with microvascular thrombosis. Following the procedure, platelet count, hemoglobin, and complement C3 returned to normal, and the wound healed without complication. At subsequent follow-up, the scars were supple and level, with no sensory deficit or functional limitation. This report expands the range of infectious triggers associated with aHUS and demonstrates that persistent necrotic cutaneous thrombotic microangiopathy may necessitate prompt surgical management in addition to complement inhibition and supportive treatment.
SN - 2296-2360
ER -